SECONDARY OA: Appears at any age in a previously damaged or congenitally abnormal joint . OA is a “wear and tear” phenomenon. Indeed the vertebrae , hips and knees are most affected . OA can be superimposed upon RHEUMATOID ARTHRITIS.

Two main theories:1)BIOMECHANICAL THEORY2)BIOCHEMICAL THEORY

This maintains the wear and tear leads to deranged function,focal death, and reactive proliferation of chondrocytes.

Collagen breakdown , fissuring and flaking and osteophyte formation occurs.

maintains that aging leads to lessened matrix maintenance and excess of lytic enzymes , which in turns lead to synovitis . Synovitis further results in a release of inflammatory mediators and cytokines(especially IL-1) , degradative enzymes and free radicals and eventually chondrocyte death.

Primary abnormality is thinning and fragmentation of the articular cartilage.

Loss of articular cartilage leads to exposure of subchondral bone , which appears as shiny foci on the articular surface( enburnation ).

New bone formation , usually in the form of nodules (spurs).

Formation of osteocartilagenous loose bodies (“joint mice”).

Inflammation is absent.

CLINICAL FEATURES:Although OA may be

asymptomatic,most patients experience morning stiffness in affected joints . There is usually no local heat or tenderness , but affected joints often show restricted range of motion , small efusions and crepitus. A slowly progressive disease characterized by joint disability.It is associated with ALKAPTONUREA and FOOTBALL PLAYERS.

OSTEOARTHRITIS IN KNEE JOINT.

OSTEOARTHRITIS.